Intervertebral Disc Degeneration

On radiography (Figure 16-1), intervertebral disc degeneration is indirectly inferred from loss of the normal disc space height. Gas may be seen in the disc space, due to a negative pressure within the degenerative disc causing extraction of nitrogen from extracellular space. This is commonly referred to as vacuum phenomenon. The vacuum phenomenon can be accentuated during extension of the spine and reduced during flexion. Vertebral endplate irregularity is often seen, with or without associated sclerotic changes at the endplates.

FIGURE 16-1 Radiographic features of degenerative disc disease.

Disc space narrowing and subtle cartilaginous endplate sclerosis are present at L4-L5.

With the wide availability of MRI, CT is rarely requested for the primary evaluation of degenerative disc disease, except in patients with contraindications for MRI examination. Similar to radiography, CT can demonstrate disc space loss, endplate irregularity or sclerotic changes, and vacuum phenomenon. However, CT also allows direct visualization of disc bulging and disc herniation (Figure 16-2), although with a lesser soft tissue contrast compared to MRI. When more accurate depiction of disc bulging and disc herniation is required, CT myelography can be performed (Figure 16-3) .

FIGURE 16-2 CT of intervertebral disc degeneration.

A, Reformatted sagittal CT image in bone window showing severe disc degeneration including severe disc space loss, lucency within the disc space consistent with gas (vacuum phenomenon), and sclerosis at the adjacent endplates (white arrow). The facet joint also demonstrates irregular hypertrophy, osteophytes and loss of joint space (open arrow). Degeneration of these structures lead to instability, resulting in anterolisthesis of L4 over L5. B, Axial image in soft tissue window demonstrates diffuse disc bulging (white arrows), thickening of the ligamentum flavum (black arrows), and facet arthropathic changes that include joint space narrowing, facet hypertrophy, and vacuum phenomenon in the facet joints (open arrow). These changes lead to severe spinal canal stenosis, with the thecal sac (T) severely compressed anteriorly and posterolaterally.

FIGURE 16-3 CT myelogram.

A, Axial image at the L3-L4 intervertebral level demonstrates a left central disc protrusion (open arrow), causing stenosis and impingement of the nerve roots at the left lateral recess. By comparison, the right L4 nerve root at right lateral recess (white arrow) is floating freely within the thecal sac. B, At the L2-L3 level, there is severe spinal stenosis as a result of disc bulging, ligamentum flavum hypertrophy, and facet arthropathic changes that include facet hypertrophy and sclerosis (circle), resulting in almost complete obliteration of the cerebrospinal fluid space (arrow).

MRI provides the best soft tissue details of degenerative disc disease. In young healthy patients, the intervertebral discs demonstrate hyperintensity on T2-weighted images. With aging, there is loss of this hyperintensity due to a decrease of water content and changes in proteoglycan composition (Figure 16-4). There is decreased disc height and the endplates may become irregular. Gas from vacuum phenomenon may fill the space of a degenerative disc, which may demonstrate hypointensity on both T1- and T2-weighted images. Alternatively, the space may be filled with fluid, which is seen as hyperintensity on T2-weighted images. A degenerative disc may also calcify, which can give hypointensity or hyperintensity on T1-weighted images, depending on the type and concentration of calcification. A degenerative disc may also enhance secondary to the presence of granulation tissues.

FIGURE 16-4 Disc degeneration seen on MRI (T2-weighted image) (same patient as Figure 16-1). There is disc space narrowing and loss of the normal T2 hyperintensity of the L4-L5 disc. Bulging of the disc with a small protrusion into the spinal canal is also shown (arrow). Compare the L4-L5 disc with the normal appearance of the discs at L2-L3 and L3-L4 levels.

Fissures of the annulus fibrosus may be seen in the intervertebral discs. On MRI, annular disruptions (also referred as fissures) may be seen as a small high intensity zone within the outer annulus (Figure 16-5) .

FIGURE 16-5 Annular disruption seen as a high intensity zone (arrow) on T2 weighted images.

One of the primary advantages of MRI is the direct visualization of disc bulging or herniation, and its associated mass effect on the nervous structures. At a particular disc level, a disc can have bulging and one or more areas of herniation seen on the same occasion. In 2001, multiple societies reached a consensus to standardize the nomenclature and classification of disc pathology.¹ This work is currently being revised (A. Williams, S. Rothman, R. Murtagh, G. Sze, in progress). The consensus was initially developed for lumbar disc disease but is generalized to disc disease in the rest of the spine. Normal disc space is defined craniocaudally by the vertebral body endplates, and circumferentially by the ring apophysis of the vertebral bodies. In the newly revised consensus, a disc bulge refers to diffuse displacement of disc material beyond the normal disc space, and covers greater than 25% of the normal disc space circumference (i.e, greater than 90 degrees of the circumference) (Figure 16-6, A) . Disc displacement covering 25% or less of the circumference is called herniation. When the width of the base of the disc herniation is greater than any other measurements in the same plane of the herniation, it is called a protrusion (Figure 16-6, B). When any of the measurements of the herniation is greater than the width at its base, the herniation is described as an extrusion (Figure 16-6, C and D). In essence, a protrusion is a disc herniation with a wide base, whereas an extrusion is a narrow-based disc herniation with appearance sometimes resembling toothpaste that is squeezed out of its container. Migration refers to herniated disc material that is displaced above or below the level of the disc. When the disc extrusion is separated from the parent disc, it is referred to as a sequestration. Sequestered disc often demonstrates T2 hyperintensity compared to its disc of origin. This may be secondary to the presence of granulation tissue, immune response, or inflammation.² Most disc sequestrations are seen in the epidural space, but rarely, they may migrate into the intradural space or posterior to the thecal sac. Herniated disc may be contained by the annulus fibrosus (subannular) or the posterior longitudinal ligament (subligamentous) (Figure 16-6, D), although the distinction sometimes can be difficult.

FIGURE 16-6 Disc bulging and herniation.

A, Diffuse disc bulging. The disc extends beyond the margin of the ring apophysis (arrows) circumferentially. B, Disc protrusion. Note the width of the base (arrow) is larger than any other dimensions of the disc herniation. Degenerative facet hypertrophy is also noted (asterisks). C, Disc extrusion. The width of the base (white arrow) is narrower than any other dimensions. The nerve root at the left lateral recess is impinged by the extruded disc. Compare this with the corresponding free nerve root on the right (open arrow). D, Subligamentous disc extrusion. Note the narrow width of the base and the location of the disc extrusion (white arrow) underneath the lifted posterior longitudinal ligament (black arrows).

Disc material can also herniate through the vertebral cartilaginous endplates into the adjacent vertebral bone marrow. Intravertebral (intraosseous) herniation is often called Schmorl’s node (Figure 16-7) and has been reported in 38% to 75% of the population. Most of these are seen as incidental findings.

FIGURE 16-7 Schmorl’s node (arrow) at superior endplate of L4 vertebra. On this sagittal T2-weighted image, loss of the normal bright signal and bulging of the L3-L4 and L4-L5 discs are also noted.

Vertebral Marrow Changes and Osteophyte Formation

Disc degeneration often leads to changes of the bone marrow adjacent to the cartilaginous endplates bordering the disc. MRI can demonstrate three patterns of bone marrow signal changes that have been classified by Modic et al³ (Figure 16-8) . The vertebral marrow changes can convert from one type to another with time. In many patients, the vertebral marrow changes actually appear in a mixed pattern. The clinical and pathophysiological significance of vertebral marrow changes have been subject to debate. Some reports have suggested that type I change is likely to be inflammatory in origin and is more strongly associated with active low back symptoms and segmental instability.⁴ It has also been suggested that patients with type I marrow changes respond better to fusion compared to those without or with other types of endplate changes, and that persistence of type I marrow changes after fusion is associated with a worse outcome.⁵

FIGURE 16-8 Degenerative vertebral endplate changes (arrows) as classified by Modic et al³ Type I marrow change demonstrates T1 hypointensity,(A) T2 hyperintensity (B) and enhances with gadolinium. (C) It represents replacement of normal hematopoietic marrow by fibrovascular tissue. Type II marrow change demonstrates hyperintensity on both T1- (D) and T2-weighted (E) images. It is secondary to conversion of hematopoietic marrow to fatty marrow. Type III change demonstrates hypointensity on both T1- (F) and T2-weighted (G) images. It represents replacement of hematopoietic marrow by sclerosis. There is no abnormal enhancement associated with type II or type III changes (not shown).

Osteophyte formation is commonly seen in the aging spine. Osteophytes refer to abnormal bony outgrowth that is believed to be induced by abnormal mechanical stress. They are often located at the edge of the annulus fibrosus and adjacent apophyses, and are best seen on radiographs or CT. Osteophytes at the outer rim of the vertebral endplates and associated with degenerative disease are commonly referred to as spondylosis deformans.

Facet Arthropathy

Degenerative changes of the facet joints in the spine resemble that of other synovial joints in the rest of the body. Although radiography can demonstrate the bone changes associated with osteoarthritis, including joint space narrowing as a result of thinning of articular cartilage, subchondral sclerosis, marginal osteophyte formation, facet hypertrophy, and hyperostosis, these findings are best demonstrated on CT (see Figures 16-2 and 16-3). Very often, gas from vacuum phenomenon can also be seen on radiography or CT. MRI does not provide as much bony detail, but facet hypertrophy is easily demonstrated (see Figure 16-6, B). In addition, MRI may demonstrate joint space effusion and inflammatory changes (synovitis) that can be associated with osteoarthritis (Figure 16-9). Synovitis is best demonstrated on fat-suppressed T2-weighted or postgadolinium MRI sequences.

FIGURE 16-9 Enhancement may be present in degenerative disease of the facet joints (arrows). Other degenerative changes of the facet joints may also include facet hypertrophy, joint space narrowing, and joint effusion.

The uncovertebral joints associated with the lower five cervical vertebral bodies are also commonly associated with arthropathic changes. The uncinate process may undergo hypertrophy and spur formation that can project into the neural foramina and spinal canal, leading to narrowing of the neuroforamina and spinal canal stenosis (Figure 16-10) .

FIGURE 16-10 Uncovertebral joint degenerative disease causing neural foraminal narrowing.

Axial CT image (A)and reformatted coronal CT image (B) at C6-C7 intervertebral level demonstrate spur formation at the uncovertebral joints (black arrows) projecting into the neural foramina, causing foraminal stenosis. Compare this with the normal uncovertebral joints at the other levels (white arrows). C, Axial T2-weighted MR image in a different patient demonstrates osteophytes at the posterior vertebral margin and uncovertebral joints (short arrows). A small disc protrusion is also noted at the left lateral recess (open arrow). There is narrowing of the bilateral neural foramina, worse on the left, causing impingement of the left exiting nerve root. Long arrow, right exiting nerve root.

Juxta-articular cysts are often seen associated with facet arthropathy. They include synovial and ganglion cysts. Compared to synovial cysts, ganglion cysts do not have synovial lining and do not communicate with the joint space. However, on imaging, it is difficult to make the distinction and they are often simply referred to as juxta-articular cysts. The cysts are usually located in the posterolateral epidural space of the spinal canal. Occasionally, they may be completely outside of the spinal canal (Figure 16-11). They can calcify and sometimes can be confused with other pathological entities such as a disc herniation or a mass. However, the recognition of continuity of a lesion with adjacent degenerative facet joint should strongly suggest the diagnosis. On MRI, their signal intensity is variable and depends on whether they contain proteinaceous material or hemorrhage. Gas may be present in synovial cysts, as they communicate with facet joints that may contain gas from vacuum phenomenon. The cyst walls may contain hemorrhage or calcification. There may be contrast enhancement in the cyst wall or surrounding soft tissues if inflammatory response is present.

FIGURE 16-11 Synovial cyst.

Axial T2-weighted MR image demonstrates degenerative changes of the bilateral facet joints, which contain a small amount of effusion. On the right; a small synovial cyst (arrow) is seen in continuity with the right facet joint.

Spondylolisthesis and Segmental Instability of the Spine

Spondylolisthesis, scoliosis, and segmental instability can result from degeneration of the stabilizing structures in the spine, including intervertebral discs, vertebral bodies, facet joints, joint capsules, and ligaments (see Figure 16-2). It is important to exclude other underlying pathologies, such as defect of the pars interarticularis or fracture. This consideration is particularly important when the anterolisthesis is greater than grade 1 (25% of the vertebral body diameter), or the degenerative changes are disproportionately mild to account for the high grade spondylolisthesis. Pars interarticularis defect can be detected using oblique radiography or CT. For occult pars defect or occult fracture, a nuclear bone scan may aid in their detection.

Segmental instability of the spine can be seen as spine deformity or spondylolisthesis that increases with spine motion and progresses over time. Standing radiography that includes anteroposterior and lateral projections with flexion and extension of the spine provides the most easily available imaging tool for evaluation of spine instability.⁶

There are currently no standardized methods or criteria for diagnosis of spine instability.⁷ However, values of 10 degrees for sagittal rotation and 4 mm for sagittal translation have been used to infer instability in some studies.⁶ Sagittal rotation is measured as the variation of angle between two opposite vertebral endplates observed during flexion and extension on lateral projection, and sagittal translation is measured as the variation of distance between the lines that follow the posterior cortices of two adjacent vertebrae. To minimize the effect of radiographic magnification, the absolute distance can be given as a percentage of the anteroposterior width of the superior vertebra.

Reproducibility of measurement of segmental instability is difficult, and is subject to many factors, including patient positioning, angulation of x-ray beam, radiographic magnification effect that varies with the distance of the anatomical structures from the x-ray detector, and patient’s level of cooperation.

Radiography can also demonstrate other indirect signs of instability, such as vacuum phenomenon and traction osteophytes. Traction osteophytes appear as horizontal osteophytes that arise typically on adjacent vertebral bodies below the rims of the endplate, approximately 2 to 3 mm from the edge of the intervertebral disc⁸ (Figure 16-12) .

FIGURE 16-12 Lateral radiography of lumbar spine demonstrates a traction spur (arrow), which is an indirect sign of segmental instability.

(From Leone A, Guglielmi G, Cassar-Pullicino VN, Bonomo L. Lumbar intervertebral instability. Radiology 2007; 245(1): 62-77, Figure 5.)

Instability is difficult to demonstrate directly on routine MRI and CT. Many imaging features can suggest instability indirectly, including spondylolisthesis, degenerative endplate changes, vacuum phenomenon, and degenerative disc disease. However, these imaging features are neither sensitive nor specific and can also be seen in degenerative spine disease without instability.

Spinal Stenosis

Spinal canal stenosis and foraminal stenosis are common consequences of degenerative disease of the spine. Patients with congenital anomalies, such as short pedicles, are particularly at risk of developing spinal stenosis. Spinal stenosis is best evaluated with MRI because of its ability to assess both bony and soft tissue structures that can narrow the spinal canal or neural foramina (Figures 16-13 and 16-14). Direct impingement on the spinal cord or nerve roots can be easily seen on MRI. Disc bulging, disc herniation, degenerative changes of the facet and uncovertebral joints, thickening of the ligamentum flavum, epidural lipomatosis and spondylolisthesis can all lead to narrowing of the spinal canal and neural foramina. Although sagittal images can provide a general overview of spinal canal stenosis, axial images are essential for an accurate assessment of the degree of stenosis.

FIGURE 16-13 Spinal canal and neuroforaminal stenosis.

A, Sagittal T2-weighted image demonstrates disc bulging at the L5-S1 level and spinal stenosis (arrow). B, Axial T2-weighted image at L5-S1 level demonstrates severe spinal stenosis with nerve root impingement as a result of congenital shortening of the pedicles (note the short distance between the facets and the vertebral body) and superimposed degenerative changes including disc bulging and facet arthropathic changes. Small arrows, disc bulging; long arrow, annular disruption; (open arrow), facet hypertrophy and joint effusion. C, Sagittal T1-weighted image in another patient demonstrates anterolisthesis of L5 over S1 secondary to spondylolysis at L5 (open arrow). The L5 nerve root exiting the L5-S1 neuroforamen is compressed (arrow). Compare this with the free L3 nerve root exiting the L3-L4 neuroforamen (open arrowhead), which is completely surrounded by normal epidural fat.

FIGURE 16-14 Severe spinal stenosis secondary to epidural lipomatosis and other degenerative changes.

A, Sagittal T1-weighted image. B, Axial T1-weighted image at L3-L4 level. C, Axial T1-weighted image at L4-L5 level. Excessive epidural fat (open arrows) in conjunction with facet hypertrophy, ligamentum flavum hypertrophy (asterisks), and disc bulging and protrusion (white arrows) result in severe spinal stenosis. The thecal sac (S) is severely compressed.

The central spinal canal can be narrowed anteriorly by disc bulge or herniation and vertebral osteophytes. Posterolaterally, it may be narrowed by facet disease and ligamentum flavum hypertrophy. Epidural lipomatosis tends to favor the posterior epidural space but may also be seen circumferentially. These abnormalities lead to distortion of the normally round or oval shape of the spinal canal and thecal sac. With worsening stenosis, the spinal canal and thecal sac may become triangularly shaped or flattened. There may be effacement of cerebrospinal fluid space located between the degenerative processes, causing spinal stenosis and impingement of the spinal cord or nerve roots.

Grading of spinal canal stenosis can be performed according to the recommendation of the Combined Task Forces of the North American Spine Society, American Society of Spine Radiology, and American Society of Neuroradiology.¹ Spinal canal compromise of less than one third of the normal canal is graded as “mild,” between one third and two thirds is “moderate,” and over two thirds is “severe.” Neural foraminal stenosis can be assessed on axial images and lateral sagittal images, using a grading scheme similar to that for central spinal canal.

Severe spinal canal stenosis can lead to compression of the spinal cord. This can result in ischemia and edema, which may eventually lead to irreversible damage and myelomalacia (Figure 16-15). Myelomalacia can be seen as T2 hyperintense signal of the spinal cord. Cystic changes and tethering of the cord to the dural sac may also be present. Differentiation of myelomalacia from reversible edema or ischemia can be difficult when atrophy associated with the myelomalacia is not evident.

FIGURE 16-15 Myelomalacia at level of C4-C5 to C5-C6 is seen as increased T2 signal (long arrow) on this sagittal T2-weighted image. The cord is atrophic with small areas of cystic changes. This patient had traumatic injury and degenerative disease of the spine. Note the disc bulging and ligamentum flavum hypertrophy at C4-C5 and C5-C6 levels (short arrows) resulting in spinal canal stenosis. There is thinning of the ligamentum flavum at C5 level (open arrow), probably from previous hyperflexion injury.